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Cited by 190Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchLipoproteins and Cardiovascular Health

Dyslipidemia and the Risk of Alzheimer’s Disease

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Reitz, Christiane·2013·Current Atherosclerosis Reports
DOI 10.1007/s11883-012-0307-3PMC PMC3564220
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Abstract

Whether cholesterol is implicated in the pathogenesis of Alzheimer's disease (AD) is still controversial. Several studies that explored the association between lipids and/or lipid-lowering treatment and AD indicate a harmful effect of dyslipidemia on AD risk. The findings are supported by genetic linkage and association studies that have clearly identified several genes involved in cholesterol metabolism or transport as AD susceptibility genes, including apolipoprotein E (APOE), apolipoprotein J (APOJ, CLU), ATP-binding cassette subfamily A member 7(ABCA7), and sortilin-related receptor (SORL1). Functional cell biology studies further support a critical involvement of lipid raft cholesterol in the modulation of Aβ precursor protein processing by β-secretase and γ-secretase resulting in altered Aβ production. However, conflicting evidence comes from epidemiological studies showing no or controversial association between dyslipidemia and AD risk, randomized clinical trials observing no beneficial effect of statin therapy, and cell biology studies suggesting that there is little exchange between circulating and brain cholesterol, that increased membrane cholesterol level is protective by inhibiting loss of membrane integrity through amyloid cytotoxicity, and that cellular cholesterol inhibits colocalization of β-secretase 1 and Aβ precursor protein in nonraft membrane domains, thereby increasing generation of plasmin, an Aβ-degrading enzyme. The aim of this article is to provide a comprehensive review of the findings of epidemiological, genetic, and cell biology studies aiming to elucidate the role of cholesterol in the pathogenesis of AD.

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  • There is a positive epidemiological correlation between Alzheimer's disease and cardiometabolic traits.

    “Studies have consistently found a positive epidemiological correlation between Alzheimer’s disease (AD) and cardiometabolic traits, yet the biological mechanisms behind this correlation is not well understood [1–4].”

    From Multi-trait association studies discover pleiotropic loci between Alzheimer’s disease and cardiometabolic traits (2021) · cites this paper as [3]

    The Conclusions say that metabolic syndrome and its individual factors have repeatedly been associated with cognitive decline and dementia, but that is broader than AD specifically. The section “Prospective Epidemiological Studies Relating Plasma Cholesterol Levels to AD” reports harmful associations for some midlife lipid measures while saying results across studies have been inconsistent. The source therefore does not support the claim that studies consistently find a positive correlation between AD and cardiometabolic traits. (LLM, conf=0.88)

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  • The biological mechanisms behind the positive epidemiological correlation between Alzheimer's disease and cardiometabolic traits are not well understood.

    “Studies have consistently found a positive epidemiological correlation between Alzheimer’s disease (AD) and cardiometabolic traits, yet the biological mechanisms behind this correlation is not well understood [1–4].”

    From Multi-trait association studies discover pleiotropic loci between Alzheimer’s disease and cardiometabolic traits (2021) · cites this paper as [3]

    The Conclusions state that mechanisms linking dyslipidemia to dementia remain unclear and that metabolic-syndrome factors have repeatedly been associated with cognitive decline and dementia. But the paper does not establish a consistently positive association between AD and cardiometabolic traits broadly; its Abstract describes epidemiological findings for dyslipidemia and AD as conflicting. (LLM, conf=0.86)

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References 114 · Cited by 190

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Authors
Reitz, C.
Affiliations
Columbia University Irving Medical Center (US)
Corresponding author
Reitz, Christiane
ORCID
Reitz, Christiane
Venue
Current Atherosclerosis Reports
Publisher
Springer Science and Business Media LLC
Published
2013-01-18
Volume
15
Issue
3
Pages
307-307
ISSN
  • 1523-3804 (ISSN-L)
  • 1534-6242
DOI
10.1007/s11883-012-0307-3
PMC
PMC3564220
OpenAlex
W2102736631
Cited by
190
References
114
Citations by year
2026: 12 · 2025: 18 · 2024: 14 · 2023: 13 · 2022: 12 · 2021: 21 · 2020: 19 · 2019: 15 · 2018: 19 · 2017: 11 · 2016: 7 · 2015: 13 · 2014: 14 · 2013: 2
FWCI
1.32
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Current Atherosclerosis Reports (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Aging (P01AG007232, K23AG034550, AG 07702, AG 07232)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Keywords
dyslipidemia, Alzheimer's disease, cholesterol, lipid metabolism, apolipoprotein E, clusterin, ABCA7, SORL1, lipid rafts, APP processing, beta-secretase, gamma-secretase, amyloid-beta, statins, genetic susceptibility, brain cholesterol
MeSH terms
Alzheimer Disease, Humans, Lipids, Prognosis, Risk Factors, Dyslipidemias, Lipid Metabolism

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